Effects of sodium houttuyfonate on expression of NF-kappaB and MCP-1 in membranous glomerulonephritis

被引:40
作者
Pan, Pei [1 ]
Wang, Yu-Jie [1 ]
Han, Lu [1 ]
Liu, Xiang [1 ]
Zhao, Meng [1 ]
Yuan, Yong-Fang [1 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Peoples Hosp 3, Dept Pharm, Shanghai 201900, Peoples R China
关键词
Glomerulonephritis; MCP-1; Nuclear factor kappa B; Sodium houttuyfonate; MONOCYTE CHEMOATTRACTANT PROTEIN-1; AP-1; ACTIVATION; TRANSCRIPTION; MECHANISMS; KIDNEYS; DISEASE;
D O I
10.1016/j.jep.2010.06.020
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Aims of the study: Sodium houttuyfonate (SH) is an addition compound of sodium bisulfite and houttuynin. Houttuynin is one of the main ingredients in the volatile oil of Houttuynia cordata Thunb, which has been widely used in traditional Chinese medicines. In this study, we investigated the effect of SH in membranous glomerulonephritis (MGN) induced by cationic Bovine Serum Albumin (C-BSA) in BALB/c mice. Materials and methods: Mice were divided into four groups, including normal vehicle-treated controls (N group), model (M group), low SH of 60 mg/kg body weight (L group), or high SH of 120 mg/kg body weight (H group). Urine protein quantification was detected by the urine protein strip test. Morphological assessment in kidneys was observed by light microscope and electron microscopy. The level of nuclear factor-kappaB (NF-kappa B) in the nuclear was evaluated by Western blot. Immunohistochemical was used to analyze the expression of MCP-1. Results: SH was shown to reverse C-BSA induced increases in urinary protein, and changes in morphology. Treatment with SH at 60-120 mg/kg (Land H groups, respectively) dose-dependently decreased the level of nuclear NF-kappa B and MCP-1 expression compared to that of the M group. Conclusions: This study reveals that SH could treat C-BSA induced MGN in BALB/c mice by suppressing NF-kappa B activation and MCP-1 expression. Therefore, the most likely mechanism underlying the biological effects of SH is inhibition of an NF-kappa B mediated-cytokine pathway. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:203 / 209
页数:7
相关论文
共 26 条
  • [1] Control of apoptosis by Rel/NF-κB transcription factors
    Barkett, M
    Gilmore, TD
    [J]. ONCOGENE, 1999, 18 (49) : 6910 - 6924
  • [2] Mechanisms of disease - Nuclear factor-kappa b - A pivotal transcription factor in chronic inflammatory diseases
    Barnes, PJ
    Larin, M
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1997, 336 (15) : 1066 - 1071
  • [3] INDUCTION OF MEMBRANOUS NEPHROPATHY IN RABBITS BY ADMINISTRATION OF AN EXOGENOUS CATIONIC ANTIGEN - DEMONSTRATION OF A PATHOGENIC ROLE FOR ELECTRICAL CHARGE
    BORDER, WA
    WARD, HJ
    KAMIL, ES
    COHEN, AH
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1982, 69 (02) : 451 - 461
  • [4] Cheung GTY, 2008, CAN J PHYSIOL PHARM, V86, P88, DOI [10.1139/Y08-002, 10.1139/y08-002]
  • [5] He Ya-ni, 2004, Zhonghua Yi Xue Za Zhi, V84, P1804
  • [6] KOSUGE T, 1952, PHARM SOC JAPAN, V72, P1227
  • [7] Li S., 1997, J SHENYANG PHARM U, V14, P144
  • [8] Preparation and suppressive effect of astragalus polysaccharide in glomerulonephritis rats
    Li, Shigang
    Zhang, Yongqi
    Zhao, Jianxiong
    [J]. INTERNATIONAL IMMUNOPHARMACOLOGY, 2007, 7 (01) : 23 - 28
  • [9] Nuclear factor-κB inhibitors as potential novel anti-inflammatory agents for the treatment of immune glomerulonephritis
    López-Franco, O
    Suzuki, Y
    Sanjuán, G
    Blanco, J
    Hernandez-Vargas, P
    Yo, Y
    Kopp, J
    Egido, J
    Gómez-Guerrero, C
    [J]. AMERICAN JOURNAL OF PATHOLOGY, 2002, 161 (04) : 1497 - 1505
  • [10] Tubular NF-κB and AP-1 activation in human proteinuric renal disease
    Mezzano, SA
    Barría, M
    Droguett, MA
    Burgos, ME
    Ardiles, LG
    Flores, C
    Egido, J
    [J]. KIDNEY INTERNATIONAL, 2001, 60 (04) : 1366 - 1377